Brenner discovered the CD1 system of lipid antigen presentation that elicits innate and adaptive immunity. His research group also investigates how inflammation induces pathological responses, including how cadherins regulate the invasion and degradation of cartilage in rheumatoid arthritis, and the role they play in chronic inflammation.

Research Interests

I work on pathways of innate and adaptive immunity. We found a new system of immune recognition mediated by CD1 molecules that enable T lymphocyte responses to lipid antigens from microbes. We are deciphering the mechanisms that determine the delivery, trafficking, processing, loading, and presentation of the lipid antigens that activate CD1 reactive T cells. These T cell responses mediate host defense by providing adaptive immunity against microbial lipid antigens, much like MHC restricted T cells do for protein antigens. A specialized subset of CD1 reactive NKT cells jump starts multiple inflammation pathways as a distinct arm of innate immunity. We are identifying the lipid antigens that stimulate these CD1 reactive T cells and their role in host defense and immunopathology. We also investigate how inflammation induces pathological responses and end-organ damage. We found that mesenchymal cadherin-11 controls the development of the joint synovium and regulates the behavior of synovial fibroblasts activated by inflammation. We are determining how cadherins regulate fibroblast mediated invasion and degradation of joint cartilage in rheumatoid arthritis, and how they impact chronic inflammation. Thus, cadherins not only mediate tissue morphogenesis in development, but also profoundly impact pathological tissue damage.

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